More MS news articles for October 1999

Jefferson researchers show melatonin's potential benefits in preventing Parkinson's damage

Contact: Steve Benowitz
Thomas Jefferson University

Melatonin could be a key to someday understanding how to treat Parkinson's disease. Scientists at Jefferson Medical College have shown in the laboratory and in test animals that melatonin is effective in preventing a particular type of brain cell damage similar to that found in Parkinson's.

Many researchers believe that the loss of dopamine nerve cells seen in Parkinson's disease patients' brains results from oxidative stress to the cells. Various cellular insults produce oxygen free-radicals, resulting in cell death. The brain's dopamine neurons are particularly vulnerable.

Melatonin, a hormone produced by the brain and which is marketed as an anti-aging agent commercially, is the body's most potent antioxidant. Two years ago, Lorraine Iacovitti, Ph.D., professor of neurology at Thomas Jefferson University in Philadelphia, and her co-workers showed in the laboratory that melatonin was effective in blocking the oxidative ravages of Parkinson's-damaged dopamine-producing cells.

Dr. Iacovitti and her team tested the theory in rats by giving the animals a toxin, 6-hydroxydopamine, which specifically damages dopamine neurons, producing a Parkinsonian-like syndrome. They found that by injecting melatonin into the rats either 10 minutes prior to the 6-hydroxy infusion or 30 minutes after, they could block the Parkinsonian effects. They were able to prevent about half of the damage, or "rescue the cells," if melatonin was given two hours later.

Dr. Iacovitti presents her team's findings October 24 at the annual meeting of the Society for Neuroscience in Miami Beach.

"If you get enough antioxidants to the dopamine nerve cells, you might be able to prevent the kinds of oxidative stress and cell death you see in Parkinson's," she says.

Dr. Iacovitti notes that melatonin "has the correct action to be developed pharmaceutically," but cautions that the dosages given to the test animals were extremely high. "Whether it could be developed into a drug is another question," she says. "It's difficult to know at what levels to keep antioxidants in the body." A drug company might be able to isolate an active part of melatonin that could be a more effective antioxidant at lower doses.

She continues to study other examples of toxin-induced Parkinsonism, some of which cause damage by other means.

She explains that in oxidative stress, cells don't automatically die. Rather, they pass through a cascade of cellular events leading to cell death. She and her team used melatonin to stop the cascade at its beginning. They would like to explore other checkpoints in the death cascade to gauge the compound's effectiveness.